Next Article in Journal
The Use of “Omics” in Lactation Research in Dairy Cows
Next Article in Special Issue
Incomplete Segregation of MSH6 Frameshift Variants with Phenotype of Lynch Syndrome
Previous Article in Journal
Melatonin Promotes the In Vitro Development of Microinjected Pronuclear Mouse Embryos via Its Anti-Oxidative and Anti-Apoptotic Effects
Previous Article in Special Issue
Transcriptomic Analysis of Calcium Remodeling in Colorectal Cancer
Open AccessArticle

AF1q Mediates Tumor Progression in Colorectal Cancer by Regulating AKT Signaling

Cancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, 1095 Jiefang Ave., Wuhan 430030, China
Author to whom correspondence should be addressed.
Academic Editor: Peter J. K. Kuppen
Int. J. Mol. Sci. 2017, 18(5), 987;
Received: 26 February 2017 / Revised: 13 April 2017 / Accepted: 2 May 2017 / Published: 5 May 2017
The up-regulation of ALL1-fused gene from chromosome 1q (AF1q) is commonly seen in aggressive hematologic malignancies as well as in several solid tumor tissues. However, its expression and intrinsic function in human colorectal cancer (CRC) remains largely undefined. To explore the role of AF1q in human CRC progression, AF1q expression was analyzed in human CRC tissue samples and CRC cell lines. Clinical specimens revealed that AF1q was up-regulated in human CRC tissues, and that this up-regulation was associated with tumor metastasis and late tumor, lymph node, metastasis (TNM) stage. AF1q knockdown by shRNA inhibited tumor cell proliferation, migration, invasion, and epithelial-mesenchymal transition in vitro, as well as tumorigenesis and liver metastasis in vivo, whereas these effects were reversed following AF1q overexpression. These AF1q-mediated effects were modulated by the protein kinase B (AKT) signaling pathway, and inhibition of AKT signaling attenuated AF1q-induced tumor promotion. Thus, AF1q contributes to CRC tumorigenesis and progression through the activation of the AKT signaling pathway. AF1q might therefore serve as a promising new target in the treatment of CRC. View Full-Text
Keywords: colorectal cancer; AF1q gene; epithelial-mesenchymal transition; metastasis colorectal cancer; AF1q gene; epithelial-mesenchymal transition; metastasis
Show Figures

Figure 1

MDPI and ACS Style

Hu, J.; Li, G.; Liu, L.; Wang, Y.; Li, X.; Gong, J. AF1q Mediates Tumor Progression in Colorectal Cancer by Regulating AKT Signaling. Int. J. Mol. Sci. 2017, 18, 987.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

Back to TopTop